Key result
Rosinidin significantly restored elevated levels of serum urea, uric acid, and creatinine, and improved oxidative stress biomarkers in rats with cisplatin-induced nephrotoxicity.
Why the study?
Molecular docking predicted rosinidin has adequate structural competency as a medicinal candidate, prompting assessment of its nephroprotective efficacy against cisplatin-induced nephrotoxicity in rats.
Does rosinidin protect against cisplatin-induced nephrotoxicity in rats?
Does rosinidin protect against cisplatin-induced nephrotoxicity in rats?
p-value: p=<0.05
Rosinidin demonstrates nephroprotective efficacy against cisplatin-induced nephrotoxicity in a rat model by modulating oxidative stress and proinflammatory biomarkers.
Supports preclinical testing of rosinidin for cisplatin nephrotoxicity; leaves open any human efficacy or safety.
BACKGROUND: . The molecular docking studies predicted that rosinidin has adequate structural competency, making it a viable medicinal candidate for the treatment of a wide range of disorders. The current study intends to assess rosinidin nephroprotective efficacy against nephrotoxicity induced by cisplatin in rats. MATERIALS AND METHODS: Oral acute toxicity tests of rosinidin were conducted to assess potential toxicity in animals, and it was shown to be safe. The nephroprotective effect of rosinidin 10, and 20 mg/kg were tested in rats for 25 days with concurrent administration of cisplatin. Several biochemical parameters were measured to support enzymatic and non-enzymatic oxidative stress such as superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH). Likewise, changes in several non-protein-nitrogenous components and blood chemistry parameters were made to support the theory linked with the pathogenesis of chemical-induced nephrotoxicity. RESULTS: Cisplatin caused significant changes in biochemical, enzymatic, and blood chemistry, which rosinidin efficiently controlled. CONCLUSIONS: The present investigation linked rosinidin with nephroprotective efficacy in experimental models.
No takes yet. Share an insight, caveat, or question.
Gilani et al. (2022) studied Cisplatin-induced nephrotoxicity (n=24). Rosinidin vs. Cisplatin control was evaluated on Serum urea, uric acid, and creatinine levels (p=<0.05). Rosinidin significantly restored elevated levels of serum urea, uric acid, and creatinine, and improved oxidative stress biomarkers in rats with cisplatin-induced nephrotoxicity.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: